动物实验,孕期炎症 z-bo 2020-09-03 412

　　It is well known that in primates and rodents, maternal immune activation (MIA) during pregnancy can lead to abnormal behaviors caused by neurodevelopmental disorders in offspring. In humans, studies have shown that embryos exposed to maternal inflammation are more likely to develop autism spectrum disorder. Previous studies in mice have shown that a molecule called interleukin 17a (a type of Th17 cells in various inflammatory states produced by a group of helper T cells) may play a role. In pregnant mice, interleukin-17a can cause abnormal behavior and cortex in the offspring of the mother when the mother mouse is immune to activation due to infection or autoinflammatory syndrome. Jun Huh of the University of Massachusetts, Gloria Choi of the Massachusetts Institute of Technology, and colleagues investigated whether maternal gut bacteria can trigger MIA-related behavioral processes in mouse offspring. The authors found that pregnant women’s gut bacteria may stimulate the production of Th17 cells during pregnancy. This means that their offspring are likely to suffer from MIA-related behavioral abnormalities. Pregnant mice with murine nodular filamentous bacteria or human symbiotic bacteria can induce intestinal Th17 cells, especially in the offspring at the risk of neurodevelopmental disorders, especially if the mother mouse is infected during pregnancy and it may increase the risk.

　　In the second paper, Choi, Huh and co-authors searched for mouse brain regions that caused abnormal behavior in the offspring of mice exposed to inflammation during pregnancy. The author has identified the area that produces this effect, namely the area around the main somatosensory cortex. The main somatosensory cortex is involved in proprioceptive functions (related to the spatial recognition of body parts). They also found that the reduction in neural activity in the primary somatosensory cortex of the offspring of mice with neurodevelopmental disorders associated with MIA was sufficient to correct the observed behavioral abnormalities. Craig Powell of the University of Texas Southwestern Medical Center said in a corresponding news and review article: "Even if there is no such mechanism in human autism, the relationship between gut bacteria, immune system, and brain development is also So." The complex interaction between them provides scientists with valuable new insights. "